Muscles
Is the End-Exercise Potentiated-Twitch Decrement a Regulated Variable? A Mechanism-Oriented Review of Muscle Fatigue During High-Intensity Aerobic Exercise
By Arnulfo Ramos‐Jiménez, Mariazel Rubio-Valles, Marina Trejo-Trejo and 5 others.
Abstract
Background
Fatigue in high-intensity exercise is often attributed to a defended ceiling of peripheral fatigue; evidence is mixed.
Objectives
We aimed to assess whether the end-exercise potentiated-twitch decrement behaves as a regulated variable across candidate mechanisms.
Methods
PubMed/MEDLINE, Scopus, and Web of Science were searched to 12 August 2026. Evidence came from controlled studies in adults, with permeabilized-fiber, rodent, and isolated-actomyosin experiments only where human measurement is impossible.
Results
Nine mechanisms met the criteria. Inorganic phosphate and hydrogen ions impair the cross-bridge cycle; reduced sarcolemmal excitability (K+) and reduced sarcoplasmic reticulum Ca2+ release reverse over minutes and days, respectively. Only the cross-bridge effects are driven by metabolites (protons, ATP, lactate) that are agonists of group III/IV afferents; the afferents do not sense contractile impairment itself. Oxygen delivery, respiratory-muscle work, substrate availability, and perceptual load altered fatigue rate more than the end-exercise value, which varied with duration, prior exercise, muscle mass, and mode.